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The cystic fibrosis transmembrane conductance regulator (CFTR) gene shows a complex mechanism of tissue-specific and temporal regulation. Expression of the sheep and humanCFTRgenes shows a gradual decline during lung development, from the early mid-trimester through to term. Alternative upstream exons ofCFTRhave been identified in several species but their functional role remains obscure. We identified a novel 5′ exon of the sheepCFTRgene (ov1a) that occurs in two splice forms (ov1aL and ov1aS), which are both mutually exclusive with exon 1.CFTRtranscripts including ov1aL and ov1aS are present at low levels in many sheep tissues, however ov1aS shows temporal and spatial regulation during fetal lung development, being most abundant whenCFTRexpression levels start to decline. Alternative 5′ exons −1a and 1a in the humanCFTRgene also show changes in expression levels through lung development. Evaluation of ov1aL and ov1aS by Mfold reveals the potential to form extremely stable secondary structures which would cause ribosomal subunit detachment. Further, the loss of exon 1 from theCFTRtranscript removes motifs that are crucial for normal trafficking of the CFTR protein. Recruitment of these alternative upstream exons may represent a novel mechanism of developmental regulation ofCFTRexpression.

Alternative 5′ exons of the CFTR gene show developmental regulation